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The Journal of Emergency Medicine, Vol. 42, No. 1, pp. 62–64, 2012Copyright © 2012 Elsevier Inc.

Printed in the USA. All rights reserved0736-4679/$–see front matter

doi:10.1016/j.jemermed.2009.08.003

Visual Diagnosis inEmergency Medicine

ULCERS IN THE EYE

Daniel Morris, MD* and Emi Latham, MD*†

*Department of Emergency Medicine and †Hyperbaric Medicine Center, University of California, San Diego Medical Center,San Diego, California

Reprint Address: Daniel Morris, MD, Department of Emergency Medicine, University of California, San Diego Medical Center, 200 W.

Arbor Drive, San Diego, CA 92103

O

INTRODUCTION

Corneal ulcerations are a common finding in patientspresenting to the Emergency Department (ED) with apainful irritated eye. There are numerous etiologies forcorneal ulcers, and differentiating between these etiolo-gies can alter the management of the patient. We willdiscuss the diagnoses in two cases of corneal ulcerationthat presented to the ED with unilateral painful red eye.The appearance of the face and neurologic examinationswere the same for both patients, and the important dis-tinctions between the 2 patients were possible only onthe slit lamp examination. Based on the results of the EDslit lamp examination, the patients were diagnosed withdifferent etiologies for their corneal ulcers and weretreated as indicated.

DISCUSSION

For Case #1, a true dendritic ulcer pattern can be seen(Figure 1), and the diagnosis of herpes simplex keratitiswas made. In Case #2, a pseudodentritic pattern (Figure2) was seen that led to the diagnosis of herpes zosterophthalmicus.

Photographs were taken by Diana Shiba, MD, Resident, De-partment of Ophthalmology, UCSD Medical Center, San Di-ego, CA.

RECEIVED: 20 May 2009; FINAL SUBMISSION RECEIVED: 14

CCEPTED: 2 August 2009

62

Herpes Simplex Virus Keratitis: Figure 1

Herpes simplex virus (HSV) keratitis results from activeviral replication within the corneal epithelium (1). It isthe most common cause of corneal ulceration and cor-neal cause of blindness in the United States. Most infec-tions are caused by HSV type 1, however, in occasionalcases it can be caused by HSV type 2 (1). The lesions andclinical presentation do not differ between the two types.Herpetic keratitis as seen in Case 1 results from reacti-

009;

Figure 1. Case #1: dendritic ulcer pattern. The arrow pointsto the pattern, which is seen in infections by herpes simplexvirus. The ulcers are branching and form a fern-like pattern.Photos taken by Diana Shiba, MD, Resident, Department of

phthalmology, UCSD Medical Center.

July 2

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Ulcers in the Eye 63

vation of the virus from an earlier infection. This reac-tivation can be triggered by fever, exposure to ultravioletlight, trauma, or other local or systemic source of im-mune suppression (1).

The first signs of viral replication in the cornea aresmall, raised, clear vesicles that are similar to the vesic-ular eruptions seen in herpes infections elsewhere in thebody. These vesicles are rarely seen or recognized duringa patient’s first presentation. However, in patients with aknown history of HSV keratitis, these vesicles can beseen in the absence of any clinical symptoms (2).

Within several hours, these corneal vesicles coalesceinto a dendritic pattern. As the disease progresses, acentral epithelial defect develops. The resultant dendriticulcer is the most common presentation of HSV keratitis (2).

Prominent features of a HSV dendritic ulcer includebranching terminal bulbs, swollen epithelial borders thatcontain live viruses, and central ulceration through thebasement membrane (2). If the ulcer enlarges, its shape isno longer linear. At this point it is referred to as ageographic ulcer (2).

Most cases of HSV epithelial keratitis resolve spon-taneously within 3 weeks. The purpose of treatment is tominimize stromal damage and scarring. Antiviral ther-apy, topical or oral, is an effective treatment (1). Eithertopical trifluridine 1% solution eight times daily or vi-darabine 3% ointment five times daily has equal efficacyin treating a dendritic ulcer; however, trifluridine is moreeffective than vidarabine for treatment of a geographiculcer (3–5). Response to topical therapy usually occurs in2–5 days, with complete resolution in 2 weeks. Ophthal-mology consultation is recommended in combination

Figure 2. Case #2: pseudodendritic ulcer pattern. The arrowpoints to the pattern, which is seen in infections by herpeszoster virus. The pseudodentritic ulcers are linear withoutbranching. Photos taken by Diana Shiba, MD, Resident, De-partment of Ophthalmology, UCSD Medical Center.

with antiviral therapy. Corneal toxicity is a common b

adverse effect of topical antiviral agents (3–5). There-fore, topical therapy should be tapered rapidly after ini-tial response and discontinued after complete healing,generally within 10–14 days. Failure of epithelial heal-ing after 2–3 weeks of antiviral therapy suggests epithe-lial toxicity, neurotrophic keratopathy, or, rarely, drug-resistant strains of HSV. Vidarabine is often effectiveagainst HSV strains that are resistant to trifluridine andacyclovir (4,5).

Oral acyclovir (2 g/day) has been reported to be aseffective as topical antivirals, with the added advantageof no ocular toxicity. Newer oral antiviral drugs, such asvalacyclovir and famciclovir, further simplify the dosingregimens; however, the optimal dose for ocular diseasehas not been determined.

Topical corticosteroids are contraindicated in thetreatment of HSV keratitis, as they can increase viralreplication and expand the lesions (1).

Herpes Zoster Ophthalmicus: (Figure 2)

The dendritic pattern seen in HSV infection is not seenwith zoster infection. Pseudodendrites, which onlyvaguely resemble true dendrites, are present. Loss ofcorneal sensation is a prominent feature of zoster infec-tion (1). Unlike HSV keratitis that usually only affectsthe epithelium, varicella zoster virus (VZV) keratitisaffects the stroma and anterior uvea at onset (1).

A Tzanck smear and Wright stain can be performed,however, such tests do not distinguish VZV from otherherpes viruses (6). Viral culture or direct immunofluores-cence assay can be used to make a definitive diagnosis, asthese will differentiate VZV from other herpes viruses (6).

Care of herpes zoster ophthalmicus includes localound care, adequate analgesia, antiviral agents, and

ntibiotics for secondary bacterial infection (1,2,7,8).hen the blinking reflex and eyelid function are com-

romised, an eye lubricant is needed to prevent cornealesiccation injury. Oral acyclovir has been shown tohorten the duration of signs and symptoms, as well as toeduce the incidence and severity of complications (9).cyclovir seems to most benefit patients whose therapy

s initiated within 72 h of onset of the skin lesions, withigher complication rates occurring among patientshose treatment was delayed (9). Both famciclovir andalacyclovir (500 mg three times a day) have beenhown to be as effective as acyclovir (800 mg five timesday) in the treatment of herpes zoster and reduction in

omplications (10,11). These medications have simplerosing regimens than acyclovir, which may increaseatient compliance. The standard duration of antiviralherapy is 7–10 days. Nevertheless, the VZV DNA had

een shown to persist in the cornea for up to 30 days.

64 D. Morris and E. Latham

Unlike HSV keratitis, the role of topical antivirals is lesscertain. Additionally, topical corticosteroids may beneeded to treat severe keratitis, uveitis, and secondaryglaucoma (1,12).

Ophthalmology consultation is suggested for any caseof suspected HSV keratitis or herpes zoster ophthalmicus.

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